Distributive Shock

Definition

Shock can be classified into four states: hypovolemic, cardiogenic, obstructive, and distributive. Of the four, distributive shock is the most common condition encountered in the critical care setting. Distributive, or vasodilatory, shock is characterized by the shunting of oxygen transport to the tissues, resulting in abnormal distribution of tissue perfusion and impaired regional oxygen extraction. In contrast to the other categories of shock, this classically occurs in the presence of normal or increased cardiac output.

The diagnosis of distributive shock should include the following:

• 1.

  Systolic blood pressure less than 90 mm Hg or mean arterial pressure (MAP) less than 65 mm Hg for at least 30 minutes.

• 2.

  Normal or high cardiac index (≥2.0 L/min per m ² ). It is important to note that although distributive shock is typically characterized by high cardiac output, it is a state that may result in transient myocardial depression or may occur in a patient with underlying left ventricular dysfunction.

• 3.

  Tissue hypoperfusion manifested by oliguria (<0.5 mL/kg per hour), altered mental status, elevated lactate (>2 mmol/L).

Etiology

Distributive shock can be further categorized into its different causes. Septic shock is the classic form of distributive shock, as it is the most prevalent type of shock encountered in the ICU. Septic shock occurs as a result of an infection that induces circulatory dysfunction in the host. Neurogenic shock is a form of distributive shock that occurs in patients with severe traumatic brain injury and spinal cord injury that result in autonomic dysfunction. Anaphylactic shock results from a serious immunoglobulin E (IgE)-mediated reaction to an allergen. Distributive shock may also occur as a component of the systemic inflammatory state encountered in patients with a large acute MI. Other less common causes of distributive shock include postcardiac arrest, pancreatitis, drug or toxin reactions, burns, air or fat embolism, adrenal crisis, and thyrotoxicosis.

Incidence

Of the different types of shock, septic shock is most commonly encountered in the ICU. In an analysis of 1600 patients who presented with shock, septic shock occurred in 62%, cardiogenic shock in 16%, hypovolemic shock in 16%, other types of distributive shock in 4%, and obstructive shock in 2%. Rates of sepsis and septic shock have continued to increase over the years, likely due to the advancing age of the population, multidrug-resistant organisms, and the increased use of immunosuppressive agents. An emphasis on the earlier detection of sepsis may contribute to this increase as well. While four discrete classifications of shock are described, it is important to recognize that a substantial number of patients may present with “mixed” or multifactorial states of shock. The overlapping features of these presentations make it challenging to determine the definitive diagnosis and subsequent management.

Pathophysiology

Circulatory shock is characterized by a severe deficiency in oxygen delivery and failure of tissue perfusion. Depending on the etiology of the shock state, this can occur through a variety of mechanisms. The end result is the critical impairment of oxidative metabolism, ultimately leading to organ failure and death. It is important to identify the etiology of the shock and its underlying pathophysiology in order to manage it rapidly and effectively.

The microcirculation may be considered its own organ system, consisting of a complex network of vessels involved in the delivery of oxygen to cells. A variety of factors influence the microcirculatory system. In distributive shock, abnormalities in the microcirculation lead to significant peripheral vasodilatation and impairment of autoregulatory mechanisms required to maintain adequate tissue perfusion. Multiple mechanisms contribute to the microcirculatory derangements ( Fig. 21.2 ). Endothelial cells become more leaky and less responsive to vasoactive agents. Inflammatory activation leads to upregulation of the nitric oxygen (NO) system, resulting in shunting of blood flow within the microcirculation. An imbalance of vasoactive substances also contributes to alterations in blood flow and, thus, a regional mismatch in oxygen supply and demand. Additionally, both the activation of the coagulation cascade and the reduced deformability of erythrocytes and leukocytes lead to microvascular plugging, further compromising capillary flow. Blood flow is shunted away from the vital organs, resulting in tissue hypoxia. The uneven distribution of microcirculatory blood flow can result in impaired oxygen delivery even when patients are normotensive.

The prototype of distributive shock is septic shock. In septic shock, the interaction between the microorganism and the host immune system creates an exaggerated inflammatory response. The systemic overexpression of inflammatory mediators, such as tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), lead to microcirculatory dysfunction and ineffective distribution of blood flow away from vital organs. Aside from deficient oxygen delivery, mitochondrial dysfunction within the cells—that is, cytopathic hypoxia—contributes to inadequate oxygen utilization as well. In addition, inflammatory cytokines activate the coagulation cascade, inducing a procoagulable state that may subsequently lead to disseminated intravascular coagulation (DIC). While septic shock typically manifests as a hyperdynamic state with high cardiac output, the cytokines and endotoxins activated in sepsis cause myocardial depression. This sepsis-induced cardiomyopathy is characterized by ventricular dilatation, reduction in contractility, and depressed ejection fraction. The cardiomyopathy is typically reversible and resolves within 7 to 10 days.

Anaphylactic shock is mediated by a systemic IgE-mediated allergic reaction. This occurs when the patient is sensitized to a particular antigen, resulting in the production of IgE specific to that antigen. Upon reexposure to the allergen, IgE on mast cells and basophils recognizes the antigen and activates a cascade of inflammatory mediators. These mediators cause endothelial injury, cellular edema, and smooth muscle contraction. This is manifested by excessive peripheral vasodilatation and capillary leakage. Properties of other types of shock may contribute as well, such as cardiogenic shock from decreased myocardial contractility and obstructive shock from pulmonary vasospasm.

In neurogenic shock, injury to the spinal cord or brain that affects the sympathetic nervous system leads to severe autonomic dysregulation. Peripheral vasodilatation results, manifesting as hypotension. This is classically accompanied by bradycardia, as there is unopposed parasympathetic activation in the setting of sympathetic denervation.